g , β-defensins) which were effective

in blocking the mor

g., β-defensins) which were effective

in blocking the morphological shift of Candida from yeast to hyphae [41, 42]. Thus KSL-W may possibly contribute to the control of C. albicans infection by reducing cell growth and yeast-hyphae transition. The effect of KSL-W on C. albicans growth can occur either through cytolysis BIBW2992 cell line or cell membrane disruption, resulting in cell death similar to what has been demonstrated with histatin-5 [43, 44]. Indeed, it was shown that histatin-5 induces the selective leakage of intracellular ions and ATP from yeast cells. This is caused by the translocation of histatin-5 into the intracellular compartment and accumulates to a critical concentration [45]. Further studies are thus

warranted to shed light on the fungicidal mechanism of KSL-W. C. albicans growth and transition from blastospore to hyphal form are particularly important for biofilm formation and C. albicans virulence because a strain that is genetically manipulated to grow exclusively in the yeast form is greatly hindered in generating biofilms. In addition, a variety of C. albicans mutants known to be unable to form hyphae also show biofilm defects [46, 47]. As KSL-W significantly reduced C. albicans growth and inhibited its transition from yeast to hyphae, this suggests that KSL-W may inhibit C. albicans biofilm formation. Our findings indicate that KSL-W was indeed able to reduce biofilm formation and that its effect was comparable selleck screening library to that obtained with amphotericin B, a well-known antifungal molecule. Also of interest is that a significant

inhibition of C. albicans biofilm formation was obtained at a concentration of as low as 25 μg/ml of KSL-W antimicrobial peptide. These useful data are comparable to those of other studies showing the positive action of synthetic peptide in controlling and preventing microbial biofilm formation [48]. Thus, with its significant impact in reducing C. albicans biofilm formation, KSL-W may show potential for several novel Rabusertib applications Lck in the clinical setting. Further investigations will elucidate this effect. Biofilm formation can be controlled with anti-biofilm molecules prior to its development, although this is not actually the case in clinical applications, as antifungal and microbial molecules cannot be used on a daily basis to prevent biofilm formation. An effective molecule should ideally be able to prevent biofilm formation, but more importantly to disrupt biofilms that are already formed. We therefore questioned whether KSL-W was capable of disrupting mature C. albicans biofilm. We proceeded to examine the impact of KSL-W on mature biofilm formation and demonstrated a significant disruption of these biofilms following contact with KSL-W, thus suggesting the possible use of this antimicrobial peptide to reduce/eliminate mature biofilms.

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